• The Transactions of the Korean Institute of Electrical Engineers D
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• v.52 no.3
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• pp.134-141
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• 2003

PID controllers with constant gains have been widely used in various control systems due to its powerful performance and easy implementation. But it is difficult to have uniformly good control performance in all operating conditions. In this paper, we propose a nonlinear variable PR controller with immune feedback mechanism. An immune feedback mechanism is based on the functioning of biological T-cells, they include both an active term, which controls response speed. and an inhibitive term, which controls stabilization effect. Therefore, the proposed nonlinear PID controller is based on immune responses of biological. immune feedback mechanism which is the cell mediated immunity and In order to choose the optimal nonlinear PID controller games, we also propose the tuning algorithm of nonlinear function parameter in immune feedback mechanism. To verify performance of the proposed algorithm, the speed control of nonlinear DC motor are performed. Front the simulation results, we have found that the proposed algorithm is more superior to the conventional constant fain PID controller.

• The Transactions of the Korean Institute of Electrical Engineers D
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• v.52 no.5
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• pp.259-267
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• 2003

In this paper, we propose a nonlinear variable PID controller using a cell-mediated immune response. An immune feedback response is based on the functioning of biological T-cells. An immune feedback response and P-controller of conventional PID controllers resemble each other in role and mechanism. Therefore, we extend immune feedback mechanism to nonlinear PE controller. And in order to choose the optimal nonlinear PID controller games, we also propose the on-line tuning algorithm of nonlinear functions parameters in immune feedback mechanism. The trained parameters of nonlinear functions are adapted to the variations of the system parameters and any command velocity. And the adapted parameters obtained outputs of nonlinear functions with an optimal control performance. To verify performances of the proposed control systems, the speed control of nonlinear BC motor is performed. The simulation results show that the proposed control systems are effective in tracking a command velocity under system variations.

• Proceedings of the Korean Institute of Intelligent Systems Conference
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• 2002.12a
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• pp.113-117
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• 2002

PID controllers, which have been widely used in industry, have a simple structure and robustness to modeling error. But it is difficult to have uniformly good control performance in system parameters variation or different velocity command. In this paper, we propose a nonlinear adaptive PR controller based on an Immune feedback mechanism and a gradient descent teaming. This algorithm has a simple structure and robustness to system parameters variation. To verify performances of the proposed nonlinear adaptive PID controller, the speed control of nonlinear DC motor Is peformed. The simulation results show that the proposed control systems are effective in tracking a command velocity under system parameters variation

• Proceedings of the Korean Institute of Information and Commucation Sciences Conference
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• v.9 no.2
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• pp.701-704
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• 2005

PID controllers, which have been widely used in industry, have a simple structure and robustness to modeling error. But They are difficult to have uniformly good control performance in system parameters variation or different velocity command. In this paper, we propose a nonlinear adaptive PID controller based on a cell-mediated immune response and a gradient descent learning. This algorithm has a simple structure and robustness to system parameters variation. To verify performances of the proposed nonlinear adaptive PID controller, the speed control of nonlinear DC motor is performed. The simulation results show that the proposed control systems are effective in tracking a command velocity under system parameters variation.

• IMMUNE NETWORK
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• v.20 no.6
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• pp.49.1-49.15
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• 2020

C-C chemokine receptor type 5 (CCR5) regulates the trafficking of various immune cells to sites of infection. In this study, we showed that expression of CCR5 and its ligands was rapidly increased in the kidney after systemic Candida albicans infection, and infected CCR5^-/- mice exhibited increased mortality and morbidity, indicating that CCR5 contributes to an effective defense mechanism against systemic C. albicans infection. The susceptibility of CCR5^-/- mice to C. albicans infection was due to impaired fungal clearance, which in turn resulted in exacerbated renal inflammation and damage. CCR5-mediated recruitment of NK cells to the kidney in response to C. albicans infection was necessary for the anti-microbial activity of neutrophils, the main fungicidal effector cells. Mechanistically, C. albicans induced expression of IL-23 by CD11c⁺ dendritic cells (DCs). IL-23 in turn augmented the fungicidal activity of neutrophils through GM-CSF production by NK cells. As GM-CSF potentiated production of IL-23 in response to C. albicans, a positive feedback loop formed between NK cells and DCs seemed to function as an amplification point for host defense. Taken together, our results suggest that CCR5-mediated recruitment of NK cells to the site of fungal infection is an important step that underlies innate resistance to systemic C. albicans infection.

• Molecules and Cells
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• v.38 no.1
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• pp.26-32
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• 2015

Toll-like receptors (TLR) 7 and 9 transduce a cellular signal through the MyD88-dependent pathway and induce the production of inflammatory mediators against microbial nucleotide components. The repeated stimulation of TLR4 leads to endotoxin tolerance, but the molecular mechanisms of tolerance induced through the costimulation of individual TLR has not yet been established, although endosomal TLRs share signaling pathways with TLR4. In the present study, mouse macrophages were simultaneously stimulated with the TLR7 agonist, gardiquimod (GDQ), and the TLR9 agonist, CpG ODN 1826, to examine the mechanism and effector functions of macrophage tolerance. Compared with individual stimulation, the costimulation of both TLRs reduced the secretion of TNF-${\alpha}$ and IL-6 through the delayed activation of the NF-${\kappa}B$ pathway; notably, IL-10 remained unchanged in costimulated macrophages. This tolerance reflected the early induction of suppressor of cytokine signaling-1 (SOCS-1), according to the detection of elevated TNF-${\alpha}$ secretion and restored NF-${\kappa}B$ signaling in response to the siRNA-mediated abrogation of SOCS-1 signaling. In addition, the restimulation of each TLRs using the same ligand significantly reduced the expression of both TLRs in endosomes. These findings revealed that the costimulation of TLR7 and TLR9 induced macrophage tolerance via SOCS-1, and the restimulation of each receptor or both TLR7 and TLR9 downregulated TLR expression through a negative feedback mechanisms that protects the host from excessive inflammatory responses. Moreover, the insufficient and impaired immune response in chronic viral infection might also reflect the repeated and simultaneous stimulation of those endosomal TLRs.